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| CASE REPORT |
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| Year : 2020 | Volume
: 2
| Issue : 1 | Page : 18-20 |
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Acute Pulmonary Embolism Secondary to Pacemaker Insertion
Jay Prakash1, Rash Kujur2, Ramesh Kumar Kharwar3, Amit Kumar Gupta4
1 Department of Critical Care Medicine, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand, India
2 Orchid Medical Centre, Ranchi, Jharkhand, India
3 Department of Intensive Care Medicine, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand, India
4 Department of Critical Care Medicine, Orchid Medical Centre, Ranchi, Jharkhand, India
| Date of Submission | 23-Jul-2020 |
| Date of Acceptance | 29-Aug-2020 |
| Date of Web Publication | 31-Dec-2020 |
Correspondence Address:
Dr. Jay Prakash
C/O-R.P. Sinha, HI-166, Harmu Housing Colony, Ranchi, Jharkhand
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jtccm.jtccm_12_20
Acute pulmonary embolism is an uncommon complication after pacemaker insertion. This report describes, in view of multiple finding, we found the exact cause of the present scenario of the patient which is rare and successfully managed.
Keywords: Acute pulmonary embolism, pacemaker, management
How to cite this article:
Prakash J, Kujur R, Kharwar RK, Gupta AK. Acute Pulmonary Embolism Secondary to Pacemaker Insertion. J Transl Crit Care Med 2020;2:18-20 |
| Introduction | |  |
A pacemaker or cardiovascular implantable electronic devices (CIEDs) are commonly used for treating cardiac arrhythmias. Pacemaker implantation is related to the potential for different acute and late complications. With the bloodstream contact, an endocardial lead represents a foreign body and has a tendency to form thrombus with potential to embolize and cause a pulmonary embolism (PE).[1] Lead-related thrombi have been known to force out of position to the pulmonary circulation and for the most part, bring about asymptomatic or subclinical PE is up to 48% of cases with transvenous CIED leads.[2] Right atrial thrombosis and PE are infrequent complications of transvenous pacemaker insertion. Symptomatic PE has been reported in 0.6%–3.5% of patients.[3] We present here a case of subsequently developed PE following permanent pacemaker implantation which was successfully managed.
| Case Report | | |
An 89-year-old male weighing 55 kg was admitted to the intensive care unit (ICU) with a complaint of acute breathlessness, pain in the infra-axillary area, and bilateral swelling of the lower limb with a history of bronchial asthma. Five days back, a permanent pacemaker (Medtronic Capsure®SP Novus) had been implanted through the right subclavian vein due to complete heart block in another hospital. Laboratory data were leukocytosis with elevated liver enzymes. Chest X-ray (CXR) showed multiple opacities in right lower, left upper, and mid-zone with apparent cardiomegaly [Figure 1]. A pleural based soft lesion in the right chest wall with the destruction of the 8th rib was described. We preferred noncontrast computed tomography (NCCT) because the patient had a history of allergy with dye. NCCT of the thorax [Figure 2] was suggestive of thrombus (multiple areas of filling defects in the right ventricle and right atrium) within the right heart along with solid necrotic and cavitary lesions in both lungs and pericardial effusion. On CXR finding, computed tomography (CT)-guided fine-needle aspiration cytology of the right-sided thoracic lesion was done which was suggestive of poorly differentiated carcinoma, an unpredicted finding. | Figure 1: Chest X-ray showing multiple opacities in right lower, left upper, and mid-zone
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 | Figure 2: Noncontrast computed tomography of the thorax showing multiple areas of filling defects in the right ventricle and right atrium and pericardial effusion
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A transthoracic echocardiogram performed on the hospitalization which showed 4-cm freely mobile large mass attached to the tricuspid valve and mild pericardial effusion. With the admission, the patient received hydrocortisone 100 mg twice daily and oxygen supplement through face mask for 2 days but there was no improvement in symptoms. Our patient developed dyspnea followed by hypoxia and respiratory alkalosis (pH = 7.54, PO2 = 50 mmHg, PCO2 = 22 mmHg, and HCO3 = 20 mEq/L). Subcutaneous enoxaparin 60 mg twice daily was begun for 10 days. The right ventricle dysfunction was not appeared on follow-up echocardiography and the patient remained hemodynamically stable. The patient shifted to the general ward from ICU. Enoxaparin therapy was discontinued and the patient received low-dose low-molecular-weight heparin for another 21 days before discharge.
On first look, the patient had a history of bronchial asthma and unexpected finding of malignancy, our line of treatment was accordingly. Due to the unavailability of a technician in the lockdown period, we could not perform lung perfusion scan or venography. But with radiological findings, we deferred our treatment plan and switch over to enoxaparin. Our patient was subsequently improving. Our case is unique because, in view of multiple finding, we found the exact cause of the present scenario of the patient which is rare.
| Discussion | | |
The consequences of thrombosis on pacemaker leads are potentially severe. Although PE is rare but can be fatal if it occurs. The diagnosis should be considered in pacemaker recipients who present with hemodynamic instability with chest pain or shortness of breath. Pacemaker leads, a kind of foreign body, alter venous flow, and turbulence[4] which may lead to platelet aggregation and fibrin deposition and ultimately venous occlusion. PE may happen in various clinical circumstances, for example, during the insertion and removal of central venous catheters and invasive surgical or medical procedures. In patients with advanced chronic diseases, especially with malignancies, risk of PE is relatively high. Most patients with malignancy have blood coagulation test abnormalities indicative of up-regulation of the coagulation cascade, increased platelet activation and aggregation. However, in lung metastases and lung injury secondary to radiotherapy and/or chemotherapy, diagnosis of PE may be hampered. In this patient, coagulation profile was within normal limit and malignancy was insidious finding.
Diagnostic algorithms using different noninvasive tests have been developed to determine the pretest likelihood of PE results of D-dimer assay, chest radiography electrocardiogram and CT. The mortality in untreated PE is high (30%) but appropriate treatment may decrease it to 2%–18%.[5] The intrathoracic pressure fluctuation during respiration is transmitted to the large veins in the neck and can deliver a sucking force during inspiration. This can be exaggerated by increase in inspiratory negative pressure such as anxiety, paroxysm of coughing, and chronic lung disease. Furthermore, the absence of normal venous valve in in the internal and external jugular veins may increase the chances of aspiration of large volumes of air. After pacemaker/CIEDs implantation, time of appearance of occlusion manifestations ranges from a few days to quite a long while. In this patient, clinical signs appeared 5 days after pacemaker implantation and risk factors such as malignancy was also associated. On literature search,[3],[6] along with clinical findings, we made the possibility of PE secondary to pacemaker insertion. On disappearance of symptoms with anticoagulant therapy strongly suggest the PE. The diagnosis should be considered in pacemaker recipients who experience hemodynamic decompensation with chest pain or shortness of breath. Transthoracic echocardiography and ventilation-perfusion scans are significant diagnostic tools while thinking about this finding.
| Conclusion | | |
Treatment modalities include anticoagulation, thrombolysis, and surgery, either individually or a combination of these. The decision regarding which treatment plan to use should be individualized.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Coleman DB, DeBarr DM, Morales DL, Spotnitz HM. Pacemaker lead thrombosis treated with atrial thrombectomy and biventricular pacemaker and defibrillator insertion. Ann Thorac Surg 2004;78:e83-4.  |
| 2. | Silva Marques J, Varela MG, Ferreira R, Nobre A, Almeida AG, de Sousa J. Intracardiac sterile pacemaker lead thrombosis. Rev Esp Cardiol (Engl Ed) 2012;65:193-4. |
| 3. | Noheria A, Ponamgi SP, Desimone CV, Vaidya VR, Aakre CA, Ebrille E, et al. Pulmonary embolism in patients with transvenous cardiac implantable electronic device leads. Europace 2016;18:246-52. |
| 4. | Palatianos GM, Dewanjee MK, Panoutsopoulos G, Kapadvanjwala M, Novak S, Sfakianakis GN. Comparative thrombogenicity of pacemaker leads. Pacing Clin Electrophysiol 1994;17:141-5. |
| 5. | Biedka M, Zióókowska E, Windorbska W. Acute pulmonary embolus in the course of cancer. Contemp Oncol (Pozn) 2012;16:388-93. |
| 6. | Khalameizer V, Polishchuk I, Pancheva N, Jafari J, Scharf S, Reisin L, et al. Multiple-vein thrombosis and pulmonary embolism after pacemaker implantation treated by thrombolysis. Europace 2004;6:453-6. |
[Figure 1], [Figure 2]
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